Identification of a prefrontal cortex-to-amygdala pathway for chronic stress-induced anxiety

Dysregulated prefrontal control over amygdala is engaged in the pathogenesis of psychiatric diseases including depression and anxiety disorders. Here we show that, in a rodent anxiety model induced by chronic restraint stress (CRS), the dysregulation occurs in basolateral amygdala projection neurons...

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Bibliographic Details
Published in:Nature communications Vol. 11; no. 1; pp. 2221 - 15
Main Authors: Liu, Wei-Zhu, Zhang, Wen-Hua, Zheng, Zhi-Heng, Zou, Jia-Xin, Liu, Xiao-Xuan, Huang, Shou-He, You, Wen-Jie, He, Ye, Zhang, Jun-Yu, Wang, Xiao-Dong, Pan, Bing-Xing
Format: Journal Article
Language:English
Published: London Nature Publishing Group UK 06.05.2020
Nature Publishing Group
Nature Portfolio
Subjects:
13/51
14/19
14/34
631/378
631/443
64/60
9/74
Amygdala
Amygdala - physiology
Animals
Anxiety
Anxiety - metabolism
Anxiety - physiopathology
Anxiety disorders
Basolateral Nuclear Complex - physiology
Corticosterone - pharmacology
Disorders
Etiology
Glutamic Acid - metabolism
Humanities and Social Sciences
Male
Mental disorders
Mice
Mice, Inbred C57BL
multidisciplinary
Neural Pathways - physiology
Neurons
Neurons - metabolism
Optogenetics
Pathogenesis
Prefrontal cortex
Prefrontal Cortex - physiology
Restraint, Physical
Science
Science (multidisciplinary)
Stress
Stress, Psychological
ISSN:2041-1723, 2041-1723
Online Access:Get full text
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Summary:Dysregulated prefrontal control over amygdala is engaged in the pathogenesis of psychiatric diseases including depression and anxiety disorders. Here we show that, in a rodent anxiety model induced by chronic restraint stress (CRS), the dysregulation occurs in basolateral amygdala projection neurons receiving mono-directional inputs from dorsomedial prefrontal cortex (dmPFC→BLA PNs) rather than those reciprocally connected with dmPFC (dmPFC↔BLA PNs). Specifically, CRS shifts the dmPFC-driven excitatory-inhibitory balance towards excitation in the former, but not latter population. Such specificity is preferential to connections made by dmPFC, caused by enhanced presynaptic glutamate release, and highly correlated with the increased anxiety-like behavior in stressed mice. Importantly, low-frequency optogenetic stimulation of dmPFC afferents in BLA normalizes the enhanced prefrontal glutamate release onto dmPFC→BLA PNs and lastingly attenuates CRS-induced increase of anxiety-like behavior. Our findings thus reveal a target cell-based dysregulation of mPFC-to-amygdala transmission for stress-induced anxiety. Dysregulated prefrontal control over amygdala has been implicated in the etiology of stress-related psychiatric disorders. Here, the authors show that the dysregulation preferentially occurs in amygdala neurons that are mono- but not bi-directionally connected with dorsomedial prefrontal cortex.
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ISSN:2041-1723
2041-1723
DOI:10.1038/s41467-020-15920-7